A number of important endogenous small ligands (e.g. tryptophan) as well as many drugs (e.g., phenytoin, phenylbutazone, salicylates) are carried in plasma highly bound to albumin. The albumin in plasma of patients with renal failure binds these ligands much less tightly with consequent changes in the plasma kinetics, metabolism and effects of these ligands. The overall goal of the project is to determine whether the carrier protein itself is intrinsically abnormal in uremia or is made abnormal by retained inhibitors. If the latter is the case, these uremic inhibitors will be isolated and characterized. The micro-forms of albumin as well as certain key properties (e.g., sulfhydryl content) will be compared in normal and uremic plasma, before and after procedures designed to normalize binding.